ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR864/008/SRR8645868/SRR8645868.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR864/005/SRR8645865/SRR8645865.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR864/007/SRR8645867/SRR8645867.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/SRR864/006/SRR8645866/SRR8645866.fastq.gzprimaryOK200GenomicsBiochemistry and Molecular Genetics, University of Colorado School of Medicinehttps://www.ebi.ac.uk/ena/browser/view/PRJNA524710Mus musculusA known human SNP in the matrix-binding domain of extracellular superoxide dismutase (EC-SOD), with an arginine to glycine substitution at position 213 (R213G), redistributes EC-SOD from the matrix into extracellular fluids. We reported that, following bleomycin (bleo), knock-in mice harboring the human R213G SNP (R213G mice), compared to wild-type (WT) littermates exhibit enhanced resolution of inflammation and protection against fibrosis. We tested the hypothesis that the EC-SOD R213G SNP promotes resolution via accelerated apoptosis of recruited alveolar macrophage (recAM). Overall design: RNA-seq of alveolar macrophages populations in response to bleomycinxref:PubMed:31560857ENAfalseRedistribution of EC-SOD due to the R213G SNP reveals differential RNA-seq profile of recruited alveolar macrophages and accelerated apoptosis in response to bleomycinRedistribution of EC-SOD due to the R213G SNP reveals differential RNA-seq profile of recruited alveolar macrophages and accelerated apoptosis in response to bleomycin2025-09-242022-02-03PRJNA524710GSE1273451009031560857